AIM:To evaluate the role of positron emission tomography using 18F-fluorodeoxyglucose (FDG-PET) in the surgical management of patients with pancreatic cancer, including the diagnosis, staging, and selection of patients for the subsequent surgical treatment. METHODS:This study involved 53 patients with proven primary pancreatic cancer. The sensitivity of diagnosing the primary cancer was examined for FDG-PET, CT, cytological examination of the bile or pancreatic juice, and the serum levels of carcinoembrionic antigens (CEA) and carbohydrate antigen 19-9 (CA19-9). Next, the accuracy of staging was compared between FDG-PET and CT. Finally, FDG-PET was analyzed semiquantitatively using the standard uptake value (SUV). The impact of the SUV on patient management was evaluated by examining the correlations between the SUV and the histological findings of cancer. RESULTS:The sensitivity of FDG-PET, CT, cytological examination of the bile or pancreatic juice, and the serum levels of CEA and CA19-9 were 92.5%, 88.7%, 46.4%, 37.7% and 69.8%, respectively. In staging, FDG-PET was superior to CT only in diagnosing distant disease (bone metastasis). For local staging, the sensitivity of CT was better than that of FDG-PET. The SUV did not correlate with the pTNM stage, grades, invasions to the vessels and nerve, or with the size of the tumor. However, there was a statistically significant difference (4.6 ± 2.9 vs 7.8 ± 4.5, P = 0.024) in the SUV between patients with respectable and unresectable disease.CONCLUSION: FDG-PET is thus considered to be useful in the diagnosis of pancreatic cancer. However, regarding the staging of the disease, FDG-PET is not considered to be a sufficiently accurate diagnostic modality. Although the SUV does not correlate with the patho-histological prognostic factors, it may be useful in selecting patients who should undergo subsequent surgical treatment.

Gliomatosis cerebri is a rare condition in which an infiltrative glial neoplasm spreads through the brain with preservation of the underlying structure. CT and MRI show diffuse abnormal density or signal, without mass effect, and because these findings are nonspecific, it is difficult to make a definitive diagnosis. Our purpose was to assess the usefulness of a new tumour-detecting amino acid tracer for positron-emission tomography (PET), L-[3-(18)F] alpha-methyl tyrosine (FMT), in patients with gliomatosis cerebri. We performed FMT PET, fluorodeoxyglucose FDG PET and MRI eight patients with gliomatosis cerebri and six with non-neoplastic disease, whose MRI also showed diffuse high signal on T2-weighted images. Standardised uptake (SUV) of FMT and FDG in the area of gliomatosis was obtained and the tumour-to-normal cortex (T/N) ratio of this was compared. The tumours were shown on FMT PET as areas of increased uptake, except in one patient with severe intracranial hypertension. There were significant differences between the SUV of FMT and the T/N ratio of FMT in patients and in controls (both P<0.01), and between the T/N ratio of FMT and FDG in patients ( P<0.01). Increased uptake of FMT PET strongly suggests neoplasia. FMT PET is valuable for differentiating gliomatosis cerebri from non-neoplastic diseases showing similar diffuse high signal on T2-weighted images and little contrast enhancement.

When bovine follicular fluid (BFF) was given i.p. three times at intervals of 3 h from 17.00 to 23.00 h to dioestrous rats pretreated with 10 i.u. human chorionic gonadotrophin (HCG) at 17.00 h on the day of dioestrus (day 0), the selective surge of FSH at 02.00 h on day 1 was suppressed in a dose-dependent manner. Three i.p. injections of 0.5 ml BFF completely suppressed the FSH rise in plasma at 02.00 h on day 1, but the time of premature ovulation induced by HCG was not altered. In these animals treated with HCG and BFF, however, the selective surge of FSH occurred as a delayed surge from 05.00 to 23.00 h on day 1. After seven i.p. injections of 0.5 ml BFF (from 17.00 h on day 0 to 11.00 h on day 1) the delayed surge of FSH took place from 17.00 h on day 1 to 11.00 h on day 2, indicating that waning of BFF with a decrease in inhibin secretion by the ovaries may be responsible for the delay of the FSH surge. The next spontaneous ovulation in rats treated with HCG and BFF occurred on day 5, a delay of ovulation of 1 day compared with animals given HCG on day 0 with no BFF. Initiation of follicular maturation or selection of growing follicles for the succeeding oestrous cycle appeared to be retarded by the delay of the FSH surge in HCG- and BFF-treated animals. The pituitary content of FSH in animals given HCG and three i.p. injections of 0.5 ml BFF increased strikingly until 11.00 h on day 1, when the delayed FSH surge was already in progress. These results suggest that the ability of the pituitary gland to synthesize FSH is high during the period of ovulation.

The present investigation was performed to elucidate the mechanism of the initiation of follicular maturation after inhibition of ovulation in rats treated with pentobarbitone sodium at 13.30 h and progesterone at 14.00 h on the day of pro-oestrus (day 0 denotes the day of these treatments). Ovulation was completely inhibited and the next spontaneous ovulation occurred on day 5, the expected day of the next oestrus. Follicular responsiveness to injection of human chorionic gonadotrophin (hCG) indicated that preovulatory follicles at the time of treatment with pentobarbitone and progesterone regressed by 05.00 h on day 2. Maturation of a new set of follicles began from 17.00 h on day 2 and all rats were induced to ovulate by hCG injection by 17.00 h on day 3, the number of oocytes ovulated being comparable to normal ovulation. In the animals receiving pentobarbitone sodium and progesterone treatment, two selective rises in plasma FSH, which had peak levels at 05.00 h on day 1 and 11.00 h on day 2, were observed without a rise in LH. Preovulatory surges of FSH and LH occurred on the afternoon of day 4. These results suggest that the second rise in FSH was induced by regression of Graafian follicles present at the time of treatment with pentobarbitone sodium and progesterone and that this surge of FSH was responsible for initiation of maturation of a new set of follicles destined to ovulate in the subsequent cycle. The mechanism of induction and the role of the first rise of FSH from the night of day 0 to the morning of day 1 cannot be explained at present.

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